Hemolytic Anemia Caused by Babesia microti among Stock Farmers

1
Annisa Salsabela and 2Yudha Nurdian
1
Student, Faculty of Medicine, University of Jember, Indonesia
2
Faculty of Medicine, University of Jember, Indonesia
Corresponding author : Annisa Salsabela, belalafkuj@gmail.com; 152010101063@students.unej.ac.id

Abstract
Background
Babesia microti is a parasite in wild rodents, and most cases of babesiosis in humans caused
by B. microti are transmitted from wild rodents through Ixodes tick bites or inadvertently
during blood transfusions. The life cycle of B. microti is associated with the metagenesis and
runs with two hosts: intermediate – vertebrate, and the definitive - the tick. Protozoan
parasites reproduce asexually in the intermediate hosts, while sexual reproduction occurs in
the definitive host. The main intermediate hosts and reservoirs of these protists are rodents
(Apodemus flavicolii, Clethrionmys glaveolus, Sorex araneas). Typical final hosts and
vectors of B. microti in Europe are Ixodes ricinus and I. trianguliceps, and in North America
- I. scapularis. Animals like cattle, sheep, goats, and horses brings many people into contact
with ticks while herding the livestock pasturing on steppes. Clinical signs of human
babesiosis appear between 1 and 4 weeks from man’s prick by a tick infected with B. microti
or between 9 weeks and 6 months in the case of babesiosis after blood transfusion.
Sporozoites penetrating into the interior of the cell cause the physical, chemical, and
structural changes of cell membrane. Inside the erythrocytes sporozoites are divided into 2 - 4
merozoites, and formed in this way merozoites leave the red blood cell, causing its damage
and degradation. The effects of merogony are hemolytic anemia, thrombocytopenia,
increased number of reticulocytes, and low hematocrit. Physical and chemical changes of
membranes of vascular endothelial cells, thrombocytes and red blood cells are associated
with occlusion of the small blood vessels and the formation of blockages. In the course of
babesiosis, the characteristic signs include splenomegaly, hepatomegaly and dysfunction of
the liver, kidneys, and central nervous system. Clinical presentation ranges from the
asymptomatic patient to the more critically ill patient. The intermediate disease includes non-
specific viral - like symptoms such as chills, sweats, headache, arthralgia, anorexia, cough,
and nausea. Severe disease generally occurs in people with underlying immunosuppressive
conditions that include HIV, malignancy, immunosuppressive medication, and splenectomy.
On physical examination, jaundice, retinal infarcts, or ecchymoses and petechiae may be
noted. Diagnosis is determined by several methods. Microscopic identification is performed
using Wright’s or Giemsa stain which identify the B. microti organism. A common
morphology observed on these stains is a ring-form which has low specificity resembling the
classic “signet rings” seen in malaria. To identify the presence of B. microti the blood
samples were collected and evaluate the sera and DNA by using Indirect Fluorescent
Antibody (IFA) tests and PCR. The positive detection rates obtained using the IFA tests and
PCR assays were 7% and 3%, respectively. Genomic DNA was extracted from the blood
samples using a DNeasy Blood and Tissue Kit following the manufacturer's instructions and
was stored in 100 µl of Tris-EDTA at 20℃. Common laboratory findings consist of
thrombocytopenia, normal to decreased leukocyte count, and hemolytic anemia. Data from
2000 shows that mild to moderate disease can be treated with atovaquone and azithromycin
for 7 to 10 days with comparable results and less side effects but if there is no response to
this therapy or the disease is severe then the recommendation is to transition medical therapy
back to clindamycin and quinine. Furthermore, exchange red blood cell transfusion is an
option in patients with severe parasitemia (>5-10%) or if there is pulmonary, renal, or hepatic
compromise. The most common complications of severe babesiosis include acute respiratory
failure, congestive heart failure, DIC, liver and renal failure, and splenic rupture. The
mechanism of splenic rupture is not entirely clear but may be a result of phagocytosis of
Babesia-infected erythrocytes by splenic histiocytes in addition to sequestration of platelets
causing thrombocytopenia.

Conclusion
B.microti is a parasite in wild rodents transmitted from wild rodents through Ixodes tick
bites or inadvertently during blood transfusions. Animals like cattle, sheep, goats, and horses
brings many people into contact with ticks while herding the livestock pasturing on steppes.
Sporozoites penetrating into the interior of the cell cause the physical, chemical, and
structural changes of cell membrane. Inside the erythrocytes sporozoites are divided into 2 - 4
merozoites, and formed in this way merozoites leave the red blood cell, causing its damage
and degradation. The effects of merogony are hemolytic anemia, thrombocytopenia,
increased number of reticulocytes, and low hematocrit.

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